Two prominent infectious inflammatory diseases occurring in bovines, and prevalent in dairy cattle, are mastitis and Johne's disease.
It is generally known that bovine mastitis is an inflammatory disease of the mammary gland most often caused by infection with contagious and/or environmental pathogenic bacteria such as Escherichia coli, Staphylococcus aureus, Streptococcus agalactiae and Streptococcus dysgalactiae. Generally, mastitis is manifested as a clinical as well as subclinical disease, and in cases of chronic infection, animals may remain asymptomatic throughout their entire life and potentially infect others within the herd (Oviedo-Boyso et al. 2007).
Not only is mastitis the most prevalent disease affecting dairy cattle, it is also the most costly for the dairy industry, with economic losses attributed to decreased milk production and quality, increased labor due to treatment and herd management strategies, and premature culling of highly susceptible animals (Halasa et al. 2007). In the United Kingdom alone, mastitis is estimated to cost up to 287 euros per cow per year, and approximately 9 million euros to the dairy industry as a whole (Hillerton et al. 1992; Kossaibati and Esslemont 1997).
It is known that the etiology of mastitis is complex, involving many causal strains of bacteria, as well as a wide variety of host factors that contribute to disease susceptibility. These factors include parity, stage of lactation, nutritional state, and host genetics (Oviedo-Boyso et al. 2007; Pyorala 2002). Given the complexity of this disease's etiology, and even though multiple management strategies have been adopted to control its rate of incidence, there is currently no effective means to screen for, identify and eventually eradicate mastitis from the dairy industry.
As mentioned above, another inflammatory disease occurring prominently in ruminants is Johne's disease, a chronic inflammatory bowel disease caused by an infection with Mycobacterium avium paratuberculosis (MAP). Incidentally, Johne's disease parallels Crohn's disease in humans in many respects. Since MAP is a slow-growing intracellular pathogen, infected cattle typically remain asymptomatic for 2 to 10 years making it difficult to control Johne's disease in dairy herds (McKenna et al., 2006). During this asymptomatic period, the pathogen can be horizontally transmitted to other herd members via contaminated feces, and vertically transmitted to calves via contaminated milk and colostrum (McKenna et al., 2006).
The presence of MAP in milk also poses a zoonotic risk to humans (Waddell et al. 2008). This may be particularly relevant for individuals that are genetically predisposed to inflammatory bowel disease (IBD), since MAP has been implicated as one of several potential pathogens associated with Crohn's disease (Glasser et al., 2008). A meta-analysis of studies examining the presence of MAP in patients with Crohn's disease or ulcerative colitis for example, showed that there was a greater likelihood of detecting MAP in diseased versus healthy individuals (Feller et al., 2007). Additionally, clinical studies have also shown that anti-mycobacterial treatment of some patients with Crohn's disease can lead to pathological remission (Chamberlin et al., 2007).
Variability in the susceptibility of cattle to MAP infection is evident. In a typical commercial dairy herd where there is a consistent prevalence of MAP infection for example, it is common to find animals that remain healthy, even after several years of exposure. Additionally, there is evidence that susceptibility to MAP infection, and the development of clinical symptoms associated with Johne's disease is inherited; heritability estimates in dairy cattle have been estimated to range from 0.010 to 0.183, depending on the criteria used to diagnose MAP infection or Johne's disease (Koetz et al., 2000; Gonda et al., 2006; Mortensen et al., 2004).